Kembara Xtra - Medicine - Keratoacanthoma A solitary, quickly spreading, dome-shaped, erythematous or flesh-colored papule or nodule with a central keratinous plug, often measuring 1 to 2 cm in diameter, is the most typical type of lesion. Similar to squamous cell carcinoma (SCC) clinically and microscopically The majority are benign and resolve on their own, but lesions do have the potential for invasion and metastasis, so treatment is necessary. Other presentations include grouped, multiple, keratoacanthoma (KA) centrifugum marginatum, intraoral, subungual, regressing, nonregressing, and generally eruptive. There are three KA clinical stages: - Proliferative: the lesion grows quickly over a period of weeks to months. - Maturation/stabilization: The lesion matures and the rate of development slows. The majority of lesions go to this stage, but not all do. Involution is the spontaneous resolution of the lesion, leaving a hypopigmented, depressed scar. impacted system(s): integumentary Epidemiology: Most common on sun-exposed, hair-bearing skin, but may appear elsewhere; greatest incidence age >50 years; may occur at any age; presentation enhanced throughout the summer and early fall seasons; Most frequently among fair-skinned people; highest rates in Fitzpatrick I to III (104 cases per 100,000 people); predominance of male over female (2:1) Pathophysiology and Etiology Squamous epithelial cells proliferate to extend upward around the keratin plug and proceed downward into the dermis, followed by the invasion of elastic and collagen fibers. Derived from an abnormality causing hyperkeratosis within the follicular infundibulum. Cellular mechanism causing the hyperkeratosis is currently unknown; role of human papillomavirus (HPV) has been discussed but has no established causality. Immune cytotoxicity or terminal keratinocyte differentiation may be the cause of regression. Several etiologies have been put forth: - UV radiation - Can be brought on by laser therapy, cryotherapy, chemical peels, or surgery - Genetic predisposition: Muir-Torre syndrome, xeroderma pigmentosum, Ferguson-Smith syndrome - Viral infections: Merkel cell polyomavirus or HPV BRAF inhibitors and immunosuppression (1) - Exposure to chemical carcinogens Genetics Ferguson-Smith (AD), Witten-Zak (AD), Muir-Torre (AD), Xeroderma pigmentosum (AR), Grzybowski (sporadic), and Incontinentia pigmenti (XLD) are all examples of mutations of the p53 or H-ras genes. Fitzpatrick skin types I through III are at risk for UV exposure/damage. Trauma (usually manifests within a month of injury) includes laser resurfacing, surgery, cryotherapy, and tattoos. Smoking, tar, pitch, and other chemical carcinogens; a weakened immune system; discoid lupus erythematosus; and an HPV infection are also part of the risk factors.Prevention can be achieved by sun protection. Accompanying Conditions The patient frequently has further sun-damaged skin, such as basal cell carcinoma (SCC), solar elastosis, solar lentigines, actinic keratosis, and solar lentigines. KAs are discovered with concurrent sebaceous neoplasms and cancer of the GI and GU tracts in Muir-Torre syndrome; they may exhibit sebaceous differentiation characterized as a seboacanthoma. History The lesion initially appears as a small, lone, pink macule that quickly grows; typically reaching a diameter of 1 to 2 cm; size may vary. The size of the lesion remains steady after the proliferative period has passed. Size may shrink, indicating regression If many lesions are present, it's crucial to obtain a family history and information about recent medications or treatments. Asymptomatic, occasionally tender If sebaceous neoplasms are found, the history must be checked for indications or symptoms of GI or GU malignancies. Clinical evaluation Firm, solitary, flesh-colored or erythematous, dome-shaped papule or nodule with a central keratin plug, giving the appearance of a crater. Most frequently found on sun-exposed areas: face, neck, scalp, dorsum of upper extremities, and posterior legs. Surrounding skin and borders of lesion may display telangiectasia, atrophy, or dyspigmentation. May also appear on places not exposed to the sun, such as the buttocks, anus, subungual, and mucosal surfaces. Subungual KAs, which affect the first three digits of the hands, are extremely painful. Due to the possibility of lesion spread and metastasis, check for regional lymphadenopathy. Dermoscopy: White circles and blood spots have the highest specificity and the central keratin has the highest sensitivity to distinguish from SCC.- Unable to accurately differentiate between KA and SCC SCC, Nodular or ulcerative basal cell carcinoma, Cutaneous horn, Hypertrophic actinic keratosis, Amelanotic melanoma, Merkel cell carcinoma, Metastasis to the skin, Molluscum contagiosum, Prurigo nodularis, Verruca vulgaris, Verrucous carcinoma, Deep fungal infection, Atypical mycobacterial infection, Nodular Kaposi sarcoma, and Deep fungal infection are the Laboratory Results The best diagnostic procedure is an excisional biopsy, which includes the margin and the lesion's center. A shave biopsy might not be deep enough to tell a KA from an SCC. If an excisional biopsy is not possible, the entire lesion, including the subcutaneous fat, can be deeply shaved (saucerized). Punch biopsies should be avoided since they don't provide enough tissue to accurately depict the entire lesion. Initial examinations (lab, imaging) Imaging is not necessary for the majority of lesions. Subungual KA: radiograph of the digit to monitor for osteolysis (cup-shaped radiolucent defect) Aggressive tumors may require CT with contrast for examination of lymph nodes and MRI if there is worry about perineural invasion. Interpretation of Tests A well-defined central keratin core surrounded by well-differentiated, moderately pleomorphic, atypical squamous epithelial cells with a distinctive glassy eosinophilic cytoplasm is the pathology of the sample. Histopathology shows an epithelial lip-encircled keratin-filled crater. It may be difficult and unreliable to distinguish a KA from an SCC histologically, though immunochemical staining for the cellular protein Ki-67 may be helpful in this regard. It may be possible to see elastic and collagen fibers infiltrating the squamous epithelium. Regressing KA displays flattening and fibrosis at the base of the lesion. KAs have a greater potential than SCC to demonstrate fibrosis and intraepidermal abscesses of neutrophils and eosinophils. Management Excisional surgery combined with electrodesiccation and curettage (ED&C) is the preferred form of treatment, while there are other approaches. If you have an aggressive tumor (more than 2 cm) or lesions in your face, hands, or genitalia that need tissue sparing surgery, you might want to think about Mohs micrographic surgery. In cases where there has been perineural or perivascular invasion, Mohs micrographic surgery is the preferred course of action. Small extremity lesions (less than 2 cm) may be treated with ED&C. Immunocompromised patients should undergo surgery right away. Medication Nonsurgical therapy is a successful and reasonably priced option in those rare instances where surgery is contraindicated due to the number, size, or location of the lesions, as well as in patients with many comorbidities who are reluctant or unable to tolerate surgery. Case studies and retrospective analyses support the following therapies: - 1 to 4 treatment sessions of intralesional methotrexate (12.5 to 25.0 mg in 0.5 mL of normal saline) every two to three weeks (5)[B] Complete blood counts should be used to check for pancytopenia (5).[C]. - 3 times weekly application of 5% imiquimod cream for 11 to 13 weeks (5)[B] - Daily topical 5% 5-fluorouracil cream, cure rate of 61-28% (5)[B] - Weekly administration of 50 mg/mL of intralesional 5-fluorouracil for 3 to 8 treatment sessions; 98% cure rate (5) [B] - Intralesional IFN-2a or -2b (cure rates of 83% and 100%, respectively) (5)[B] - 100% cure rate with intralesional bleomycin (5)[B] - Oral isotretinoin, 0.5–1.0 mg/kg/day Referral If lesions are more than 2 cm, frequent, mucosal, or subungual, dermatologist should be consulted. Further Treatments Cryotherapy Argon or YAG lasers Photodynamic therapy with methyl aminolevulinic acid and red light, successful case reports but also reported aggravation after treatment Radiotherapy, primary or adjuvant: KAs may regress with low doses of radiation, but may need doses up to 25 to 50 Gy in low-dose fractions (5 to 10 Gy) for potential SCC. Erlotinib, an EGFR inhibitor, 150 mg every day for 21 days, one case report Surgical Techniques The aforementioned excisional and office-based procedures Take Action Due to the increased risk of developing new lesions or skin malignancies, patients should be examined at least once a year after the surgical site has healed or the lesion has disappeared. patient observation Skin self-exams should be regularly carried out according to specific guidelines. If the patient or family members have several KAs, check for Muir-Torre syndrome, get a colonoscopy starting at age 25, and get genitourinary cancer testing done. Patient Education Sun protection precautions include wearing dark clothing, wide-brimmed hats, long sleeves, and sunblock with an SPF of at least 30. Arc welding may produce UV radiation that is hazardous to skin, thus avoid exposure. Avoid using tar, pitch, and smoking. Prognosis: Hypopigmentation and atrophic scarring may develop during self-resolution, however they may be considerably diminished with intervention. A total of 52 out of 445 cases (12%) spontaneously regressed without therapy, and none of these cases recurred. Following medical or excisional treatment, 393 (88%) individuals reverted. 445 documented cases were not fatal or metastasized because of the KA. Recurrence of 4-8% Mucosal and subungual lesions must be treated because they do not go away on their own.
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